Pathogenesis of Human Systemic Lupus Erythematosus: A Cellular Perspective
Vaishali R. Moulton,Abel Suárez-Fueyo,Esra Meidan,Esra Meidan,Hao Li,Masayuki Mizui,George C. Tsokos +6 more
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TLDR
Novel observations have provided an improved understanding of the contribution of tissue-specific factors and associated damage, T and B lymphocytes, as well as innate immune cell subsets and their corresponding abnormalities.About:
This article is published in Trends in Molecular Medicine.The article was published on 2017-07-01 and is currently open access. It has received 288 citations till now. The article focuses on the topics: Immune dysregulation & Autoimmunity.read more
Citations
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Sex Hormones in Acquired Immunity and Autoimmune Disease.
TL;DR: The role of sex hormones particularly estrogen, in the adaptive immune response, in health, and autoimmune disease with an emphasis on systemic lupus erythematosus is focused on.
Journal ArticleDOI
Autoimmunity and organ damage in systemic lupus erythematosus
TL;DR: Tsokos reviews how the genetic, epigenetic and microbial environments influence innate and adaptive immune cells to drive immunopathology and organ damage in systemic lupus erythematosus.
Journal ArticleDOI
Th17 Cells and the IL-23/IL-17 Axis in the Pathogenesis of Periodontitis and Immune-Mediated Inflammatory Diseases
Kübra Bunte,Thomas Beikler +1 more
TL;DR: A review of the current knowledge about the differentiation of Th17 cells and the role of the IL-17/IL-23 axis in the pathogenesis of IMIDs aims to review the association of these IMIDs with periodontitis and briefly discusses the therapeutic potential of agents that modulate the IL
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Regulatory T cells in the treatment of disease
TL;DR: The current progress in modulating Treg cells in autoimmune disorders, transplantation and cancer is described to promote antitumour immunity and regression.
Journal ArticleDOI
Aberrant T Cell Signaling and Subsets in Systemic Lupus Erythematosus.
TL;DR: A better understanding of the molecular defects including signaling events and gene regulation underlying the dysfunctional T cells in SLE is necessary to pave the path for better management, therapy, and perhaps prevention of this complex disease.
References
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Identification of Tim4 as a phosphatidylserine receptor.
Masanori Miyanishi,Masanori Miyanishi,Kazutoshi Tada,Masato Koike,Yasuo Uchiyama,Toshio Kitamura,Shigekazu Nagata +6 more
TL;DR: Results indicate that Tim4 and Tim1 are phosphatidylserine receptors for the engulfment of apoptotic cells, and may also be involved in intercellular signalling in which exosomes are involved.
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CD69 acts downstream of interferon-alpha/beta to inhibit S1P1 and lymphocyte egress from lymphoid organs.
Lawrence R. Shiow,David B. Rosen,Naděžda Brdičková,Ying Xu,Jinping An,Lewis L. Lanier,Jason G. Cyster,Mehrdad Matloubian +7 more
TL;DR: Treatment with the IFN-α/β inducer polyinosine polycytidylic acid inhibited egress by a mechanism that was partly lymphocyte-intrinsic, and observations indicate that CD69 forms a complex with and negatively regulates S1P1 and that it functions downstream ofIFN- α/β, and possibly other activating stimuli, to promote lymphocyte retention in lymphoid organs.
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Toll-like receptor 7 and TLR9 dictate autoantibody specificity and have opposing inflammatory and regulatory roles in a murine model of lupus.
Sean R. Christensen,Jonathan Shupe,Kevin M. Nickerson,Michael Kashgarian,Richard A. Flavell,Mark J. Shlomchik +5 more
TL;DR: It is reported that lupus-prone mice deficient in TLR7, a receptor for ssRNA, failed to generate Abs to RNA-containing antigens (Ags) such as Smith (Sm) Ag and TLR9, and this results have important implications for TLR-directed therapy of autoimmune disease.
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Neutrophil extracellular traps enriched in oxidized mitochondrial DNA are interferogenic and contribute to lupus-like disease
Christian Lood,Luz P. Blanco,Monica M. Purmalek,Carmelo Carmona-Rivera,Suk See De Ravin,Carolyne K. Smith,Harry L. Malech,Jeffrey A. Ledbetter,Keith B. Elkon,Mariana J. Kaplan +9 more
TL;DR: Findings highlight a role for mitochondria in the generation not only of NETs but also of pro-inflammatory oxidized mitochondrial DNA in autoimmune diseases.
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Type I Interferons Keep Activated T Cells Alive
TL;DR: Since IFN-α/β are very efficiently generated in response to viral and bacterial infections, these molecules may be among the signals that the immune system uses to prevent activated T cell death during infections.
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